HHV-6 may play a significant role in patients with Bell’s Palsy

Although a leading cause of Bells’ Palsy is thought to be reactivation of latent herpes simplex virus (HSV) or varicella-zoster virus (VZV), a group from Sapienza University of Rome has found that HHV-6 was not only significantly more prevalent in saliva, the viral load was also higher in patients with Bell’s Palsy compared to controls. Furthermore, patients with the worst cases had a significantly higher viral load. These findings led the group to conclude that HHV-6 may be involved in the development of the disease, or that the underlying disease mechanism might predispose patients to HHV-6 reactivation.

The group quantified HSV-1, VZV, and HHV-6 DNA in 95 saliva samples collected from patients within 48 hours from the onset of paralysis. HSV-1, VZV, and HHV-6 were detected in 13%, 3%, and 61% of patients, respectively. While the prevalence of HHV-6 DNA did not differ significantly between patients and a control group of healthy donors, the mean viral load of HHV-6 DNA copies was >.5 log higher in the patient group.

In addition, the mean viral load of saliva HHV-6 DNA recorded in patients who had an improvement of palsy at the first visit was significantly lower than that detected in patients who showed no change or an increase in symptoms.

Patients with Bell’s Palsy are typically administered a combination of corticosteroids and antivirals specific for HSV1 and VZV such as valacyclovir. Success of valacyclovir has been limited however, which would be expected if HHV-6 plays a role. Acyclovir has little impact on HHV-6 infection, which responds to beta-herpesvirus specific drugs such as foscarnet, valganciclovir and cidofovir.

Several other small studies have similarly found HHV-6 in Bell’s Palsy patients. In 2000, Pikaranta et al found HHV-6 in 7 (35%) of 20 patients and 1 of 20 healthy controls, using a qualitative PCR. Last year, this group used a microarray to test serum and CSF samples and found HHV-6 in only 4% of 46 children with Bell’s Palsy. However, HHV-6 is a low copy number virus and extremely cell associated, so it falls below the level of detection in many microarrays conducted on acellular material. HSV-1 on the other hand is a high copy number virus, and Pikaranta et al found it in 30% of samples, while VZV was found in 11% of samples.

HHV-6A specific tropism?

An intriguing 2005 study found HHV-6A in muscle biopsy tissue in approximately one-third of both Bell’s Palsy patients and patients with Meniere’s disease (Linder 2005). No HHV-6B or herpes simplex was found in these groups. Herpesviruses have also been suggested as playing a role in Meniere’s disease (Gacek 2008).

Unfortunately, the present study did not determine whether the HHV-6 virus found in the saliva was HHV-6A or HHV-6B. Furthermore, they did not determine if any of the patients with high viral loads might have had ciHHV-6, the inherited condition that results in approximately 1% of the population being born with a copy of the HHV-6 genome integrated into the chromosome of every nucleated cell.

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The HHV-6 Foundation in a non-profit entity founded to encourage scientific exchange between investigators and to provide pilot grants for promising scientific and clinical research on the under- appreciated viruses HHV-6A and HHV-6B.

The Foundation sponsors international conferences and supports scientists and clinicians seeking to clarify the role of the two HHV-6 viruses in disease. Since HHV-6A and HHV-6B can smolder in the brain and other organs without circulating in the peripheral blood or plasma, identifying chronic infection is a challenge.